tbuckley/cabot-search huggingface dataset:
Manpower proposals
Authors: D. Roy
Journal: BMJ (1983)

<h3>Background</h3> Rotavirus is the most common cause of severe secretory diarrhoea in infants and young children globally. The rotaviral enterotoxin, NSP4, has been proposed to stimulate calcium-activated chloride channels (CaCC) on the apical plasma membrane of intestinal epithelial cells. We previously identified red wine and small molecule CaCC inhibitors. <h3>Objective</h3> To investigate the efficacy of a red wine extract and a synthetic small molecule, CaCC<sub>inh</sub>-A01, in inhibiting intestinal CaCCs and rotaviral diarrhoea. <h3>Design</h3> Inhibition of CaCC-dependent current was measured in T84 cells and mouse ileum. The effectiveness of an orally administered wine extract and CaCC<sub>inh</sub>-A01 in inhibiting diarrhoea in vivo was determined in a neonatal mouse model of rotaviral infection. <h3>Results</h3> Screening of ∼150 red wines revealed a Cabernet Sauvignon that inhibited CaCC current in T84 cells with IC<sub>50</sub> at a ∼1:200 dilution, and higher concentrations producing 100% inhibition. A &gt;1 kdalton wine extract prepared by dialysis, which retained full inhibition activity, blocked CaCC current in T84 cells and mouse intestine. In rotavirus-inoculated mice, oral administration of the wine extract prevented diarrhoea by inhibition of intestinal fluid secretion without affecting rotaviral infection. The wine extract did not inhibit the cystic fibrosis chloride channel (CFTR) in cell cultures, nor did it prevent watery stools in neonatal mice administered cholera toxin, which activates CFTR-dependent fluid secretion. CaCC<sub>inh</sub>-A01 also inhibited rotaviral diarrhoea. <h3>Conclusions</h3> Our results support a pathogenic role for enterocyte CaCCs in rotaviral diarrhoea and demonstrate the antidiarrhoeal action of CaCC inhibition by an alcohol-free, red wine extract and by a synthetic small molecule.
Bartter Syndrome
Authors: Thomas James
Journal: JAMA (1976)

<h3>To the Editor.—</h3> Drs Kurtzman and Gutierrez (234:758, 1975) made several cogent arguments in advancing a new hypothesis for a single pathophysiologic basis of Bartter syndrome. They speculate that there is a defect in active chloride transport in the loop of Henle, resulting in a loss of sodium and potassium. They suggest that this would lead to hypovolemia and consequent elevation of renin and aldosterone. This may be important for some cases of Bartter syndrome. However, in five of six patients studied with Bartter syndrome, plasma volumes were normal or greater than predicted.<sup>1</sup>In the sixth patient, the measured hypovolemia was corrected by propanolol.<sup>2</sup>These observations would invalidate the hypothesis of Drs Kurtzman and Gutierrez for these particular patients. Other hypotheses to explain hypervolemia in the five cases would need to be set forth. It is possible that there is a reset baroreceptor response in some patients. A high
An assessment of (i) cyproterone acetate and (2) ethinyloestradiol and lynoestrenol (Minilyn) in the treatment of 'idiopathic' hirsutism
Authors: J.A.R. Anderson, Margaret C.K. Browning
Journal: British Journal of Dermatology (1977)

Journal Article An assessment of (i) cyproterone acetate and (2) ethinyloestradiol and lynoestrenol (Minilyn) in the treatment of ‘idiopathic’ hirsutism Get access J.A.R. Anderson, J.A.R. Anderson University of Dundee, Dundee Search for other works by this author on: Oxford Academic Google Scholar Margaret C.K. Browning Margaret C.K. Browning University of Dundee, Dundee Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 97, Issue s15, 1 December 1977, Pages 20–21, https://doi.org/10.1111/j.1365-2133.1977.tb14306.x Published: 01 December 1977
Risk
Authors: Donna Pucciani
Journal: JAMA (2016)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
The Isolated Perfused Lung
Authors: Richard W. Niemeier
Journal: Environmental Health Perspectives (1984)

The unique nonrespiratory functions of the lungs have become more apparent in recent years. The isolated perfused lung model offers many advantages over other methods for the study of pulmonary metabolism, xenobiotic disposition and the influence of interactions among agents of different physical forms. Detailed descriptions of the experimental preparation are elements in evaluating and comparing data from various sources but these are frequently neglected. A discussion and critique of the following elements are provided in this review in order to elucidate the typical problems one might encounter in evaluating data: perfusate type, perfusion method, construction materials, ventilation method, temperature control, surgical procedure, microbiological contamination and evaluation criteria of the preparation. Examples are given where the IPL method has been applied and suggestions are made for future research efforts.
Atypical blast crisis in chronic myelogenous leukemia
Authors: N. R. Korostoff
Journal: JAMA (1981)

THE TERMINAL event of chronic myelogenous leukemia (CML) being transformed into a phase indistinguishable from acute leukemia is well recognized. In most instances, there is one preponderant morphological cell type, which usually closely resembles that of acute myelogenous leukemia.<sup>1</sup>Recent studies indicate that a diverse morphological picture may be present in the peripheral blood and bone marrow of patients with clinically and often cytogenetically documented CML in blast crisis; the preponderant cells may be erythroblastic (rubriblastic), megakaryoblastic, lymphoblastic, promyelocytic, or undifferentiated.<sup>2-4</sup>This report describes a patient with a diagnosis of CML lasting ten years and terminating with a distinctly heterogeneous blastic transformation, in which myeloblasts, erythroblasts, megakaryoblasts, and undifferentiated blast cells were seen in the peripheral blood and bone marrow. These findings, which were obtained by light and electron microscopic techniques, further support the concept that all hematopoietic elements originate from a common pluripotential stem cell. <h3>Report of</h3>
Breast cancer in relation to early use of oral contraceptives. No evidence of a latent effect
Authors: J. J. Schlesselman
Journal: JAMA (1988)

A long-term latent effect of oral contraceptives (OCs) on breast cancer risk has been suggested as an explanation for some studies' failure to detect an association between OCs and breast cancer. To address this latency hypothesis, we analyzed data on 4714 case subjects and 4540 control subjects from the population-based Cancer and Steroid Hormone Study. No support was evident for a latent effect of OCs on breast cancer risk through age 54 years: among parous women who had cumulated more than six years of OC use before their first term pregnancy, the risk of breast cancer, relative to nonusers before first term pregnancy, was 0.6 at zero to four years after first term pregnancy (95% confidence interval [CI], 0.2 to 1.8), 0.7 at five to nine years (95% CI, 0.3 to 1.7), and 1.1 at ten to 14 years (95% CI, 0.3 to 3.9). Among nulliparous women with more than six years of OC use in total, the relative risk of breast cancer, by interval from last use of OCs, was 1.3 at zero to four years (95% Cl, 0.8 to 2.0), 1.1 at five to nine years (95% CI, 0.5 to 2.0), and 0.6 at ten to 14 years (95% CI, 0.1 to 3.7). (<i>JAMA</i>1988;259:1828-1833)
The Anatomy and Surgical Treatment of Hernia. By Henry O. Marcy, A.M., M.D., LL.D., of Boston.
Journal: JAMA (1893)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Endostatin reduces vascularization, blood flow, and growth in a rat gliosarcoma
Authors: Dag R. Sorensen, Tracy-Ann Read, Torsten Porwol, Bjorn Reino Olsen, Rupert Timpl, Takako Sasaki, Per O. Iversen, Haakon B. Benestad, B. Kim Lee Sim, Rolf Bjerkvig
Journal: Neuro-Oncology (2002)

Endostatin, the 20-kDa C-terminal fragment of collagen XVIII, has previously been shown to inhibit growth and induce regression of different experimental tumors in rodents.In this study, we show that recombinant murine and human endostatin, produced in 293 EBNA cells and yeast, respectively, inhibit ectotopic as well as orthotopic growing BT 4 C n gliosarcomas in BD-IX rats.In rats in which s.c.gliomas were grown for a total of 29 days, systemic treatment with recombinant murine endostatin induced about 50% reduction of intratumoral blood ow and tumor size after only 10 days of therapy.In contrast, the blood ow to irrelevant organs was unaffected by endostatin, indicating its speci city of action.Tumors were not observed to increase in size or regrow after cessation of therapy.Furthermore, endostatin-treated rats with i.c.tumors had signi cantly longer survival time than did untreated controls.In the treated rats, endostatin therapy resulted in a reduced tumor blood vessel volume and an increased tumor cell density with an increased apoptotic index within a given tumor volume, as veri ed by ow cytometry and by staining with deoxynucleotidyltransferase-mediated dUTP nick-end labeling.This work veri es the general anti-angiogenic and antitumor effects of endostatin and indicates that the protein may also be considered as a treatment strategy for malignant brain tumors.
A nonphysician looks at medical utopia
Authors: J. D. Cooper
Journal: JAMA (1966)

The medical welfare state, should it become fact in the United States, would find little to guide it in the experiences of Sweden, Saskatchewan, Britain, Czechoslovakia, or any other land that has nationalized its health services. State medical systems in operation have made use of organizational systems and insurance plans to provide free access to medical service, regardless of ability to pay. Otherwise, they have embraced no radical technological advances in the nature and delivery of medical services. In the United States, a medical welfare state would be a mammoth systems laboratory, integrating medical research, medical education, patient care, medical-records-center management, systems-information feedback (such as medical audits and drug-effects reporting), communicable-disease-control centers, mass-screening programs, coordinated progressive referral systems (essential in an age of specialization), community organization, epidemiological surveys, and other components of the ultimate medical program in a systems society. Applied science and technology would be maximally exploited in diagnosis,
DRUGS AND DIET AND MIND AND STOMACH.
Journal: JAMA (1905)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Epidemiology and Transmission
Authors: P Mullany, Coli Allan, A Jones', Pylori Bergl, M Blaser2, A Labigne3, R Rappuoli4
Journal: Gut (1995)

When exposed to an iron-deficient environment, such as that encountered in vivo, many pathogenic bacteria synthesise low molecular weight iron chelating compounds called siderophores, which are released into the environment to scavenge iron.In addition, high molecular weight outer membrane proteins (OMPs) are induced which function as receptors for these siderophores.Alternatively, some bacteria, such as pathogenic Neisseria, exhibit inducible OMP receptors which bind lactoferrin or transferrin directly.To investigate the response of H.pylori to iron-limitation, OMPs were prepared from H.pylori grown in iron-rich and iron-limiting media.Iron-limiting medium consisted of nutrient broth with 10% horse serum plus the iron chelator ethylenediamine di-o- hydroxyphenylacetic acid (EDDA, 0.04M).Iron rich medium consisted of this same medium but with excess FeSO4 (5OuM).OMPs were prepared using sodium N-lauroyl sarcosinate (Sarkosyl) to solubilise the cytoplasmic membrane and the protein composition of these preparations were compared by SDS-PAGE.One new protein of 70-8OkDa was observed in the OMP preparation from cells grown in low iron medium.In addition, two proteins of approximately 9OkDa and 4OkDa were over- expressed, and at least two proteins were under-expressed in response to low iron, compared with cells grown in iron-rich medium.The N-terminal sequences of these proteins are being determined and will be used to design oligonucleotide probes to screen a genomic library of H.pyloni to identify the genes encoding these proteins.
Abstract 1455: Athero-protective Role of IL10 Involves Regulation of Lipid Metabolism in Macrophages
Authors: Xinbing Han, Shiro Kitamoto, Qingyu Lian, William A Boisvert
Journal: Circulation (2007)

Introduction Previous studies utilizing interleukin (IL)10-overexpressing mice and IL10-deficient mice have demonstrated an anti-atherogenic role of IL10. Internalization of modified low density lipoprotein (LDL) that leads to foam cell formation has long been considered one of the requisite initiating events in atherogenesis. We sought to determine if IL10 exerts its anti-atherogenic effect by modulating lipid metabolism in the macrophage. Methods &amp; results In lipid uptake studies, IL10 substantially stimulated Dil-acetylated (Ac)LDL uptake by 187% in murine macrophage-like RAW264.7 cells. IL10 induced the expression of SR-AII and CD36 by 15.1 fold and 6.5 fold, respectively, in macrophage-derived foam cells. Moreover, CD36 protein levels were increased by IL10, suggesting that these scavenger receptors account, at least in part, for the increase in modified LDL uptake by the macrophages. Accordingly, IL10 treatment for 24hr significantly increased cholesteryl ester content by 1.5 folds compared with untreated controls (p&lt;0.05). Interestingly, IL10 also markedly promoted ATP-binding cassette protein A1 (ABCA1)-mediated free cholesterol efflux to lipid-free apoAI acting as a cholesterol acceptor. This was peroxisome proliferator-activated receptor (PPAR)γ-dependent because specific PPARγ antagonist GW9226 completely blocked the IL10-triggered cholesterol efflux to lipid-free apoAI. In addition, expression of pro-inflammatory molecules such as TNFα, MCP-1 and iCAM-1 was dramatically inhibited by IL10 in the lipid-laden foam cells. Using immunofluorescence assay of caspase 3 fragment and TUNEL assay, we demonstrated that IL10 significantly suppressed apoptosis of foam cells (27.3 ± 2.1% for AcLDL-treated cells vs. 8.3 ± 1.0 %for AcLDL plus IL10-treated cells, n=8). Conclusion Our results indicate that IL10 can mediate both the uptake of cholesterol from modified LDL and the efflux of stored cholesterol. Therefore, IL10 may facilitate the removal of harmful atherogenic lipoprotein molecules from the vessel wall. These characteristics along with its ability to suppress the expression of inflammatory molecules and apoptosis of foam cells make IL10 a highly anti-atherogenic agent.
J Neurology, Neurosurgery &amp;amp; Psychiatry, London
Journal: JAMA (1966)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Therapeutic efficacy of sonic hedgehog protein in experimental diabetic neuropathy
Authors: Nigel A. Calcutt, Karen L. Allendoerfer, Andrew P. Mizisin, Alicia Middlemas, Jason D. Freshwater, Monica Burgers, Rigel Ranciato, Jean-Dominique Delcroix, Frederick R. Taylor, Renee Shapiro, Kathy Strauch, Henryk Dudek, Thomas M. Engber, Alphonse Galdes, Lee L. Rubin, David R. Tomlinson
Journal: Journal of Clinical Investigation (2003)

Hedgehog proteins modulate development and patterning of the embryonic nervous system. As expression of desert hedgehog and the hedgehog receptor, patched-1, persist in the postnatal and adult peripheral nerves, the hedgehog pathway may have a role in maturation and maintenance of the peripheral nervous system in normal and disease states. We measured desert hedgehog expression in the peripheral nerve of maturing diabetic rats and found that diabetes caused a significant reduction in desert hedgehog mRNA. Treating diabetic rats with a sonic hedgehog-IgG fusion protein fully restored motor- and sensory-nerve conduction velocities and maintained the axonal caliber of large myelinated fibers. Diabetes-induced deficits in retrograde transport of nerve growth factor and sciatic-nerve levels of calcitonin gene-related product and neuropeptide Y were also ameliorated by treatment with the sonic hedgehog-IgG fusion protein, as was thermal hypoalgesia in the paw. These studies implicate disruption of normal hedgehog function in the etiology of diabetes-induced peripheral-nerve dysfunction and indicate that delivery of exogenous hedgehog proteins may have therapeutic potential for the treatment of diabetic neuropathy.
QUACKERY ABROAD
Journal: JAMA (2012)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
5. Lifestyle Management:<i>Standards of Medical Care in Diabetes—2019</i>
Journal: Diabetes Care (2018)

The American Diabetes Association (ADA) "Standards of Medical Care in Diabetes" includes ADA's current clinical practice recommendations and is intended to provide the components of diabetes care, general treatment goals and guidelines, and tools to evaluate quality of care. Members of the ADA Professional Practice Committee, a multidisciplinary expert committee, are responsible for updating the Standards of Care annually, or more frequently as warranted. For a detailed description of ADA standards, statements, and reports, as well as the evidence-grading system for ADA's clinical practice recommendations, please refer to the Standards of Care Introduction Readers who wish to comment on the Standards of Care are invited to do so at professional.diabetes.org/SOC.